Brain lesions that may be found in status epilepticus patients are crossed cerebellar diaschisis, signal enhancement in pulvinar, caudate nucleus, globus pallidus, putamen, and splenium of corpus callosum, the dilation of cortical vessels on the affected side, etc.1
These brain lesions in status epilepticus patients are usually reversible, but sometimes they can be irreversible and cause a permanent damage. Crossed cerebellar diaschisis is believed to take place as a disorder in the afferent corticopontocerebellar pathway is caused by a supratentorial lesion and, as a result, blood flow and oxygen decrease in the cerebellar hemisphere of the opposite side.2
In a status epilepticus patient, glutamate is discharged continuously and it induces desensitization of gamma-aminobutyric acid type A (GABAA
) and, consequently, the excitement of neurons continues and cerebral metabolism and oxygen demand increase.3
It is believed that, as a result, regions on the corticopontocerebellar pathway that fail to meet the excessively increased cerebral metabolic demand are damaged.
While a temporal lobe epilepsy patient is in seizure, the thalamus interacts with the temporal lobe, and particularly it has been reported that the pulvinar situated on the dorsomedial aspect of the thalamus plays an important role in transduction from the cortex where the seizure takes place to other regions.4
This suggests that the corticothalamic pathway is activated during the seizure, and the thalamus forms a signaling network with the cerebral cortex of other regions and, in this way, plays an important role in causing generalized seizure. It was also reported that because there may be a network inducing epilepsy formed already between the thalamus and other cortex in a temporal lobe epilepsy patient, even if temporal lobectomy is performed the prognosis may not be favorable.4
According to some reports, an extensive region of the thalamus is activated at the early stage of status epilepticus, and pulvinar lesions are observed at the later stage of status epilepticus and are involved in the suppression of signals related to seizure.5
What is more, it was reported that the signal intensity of the pulvinar in brain MRI was different according to the severity of seizure that occurred in the cortex.6
In this way, the thalamus is believed to play an important role as a pathway in mediating seizure-related signals among the cerebral cortex.
In a study by Katramados with 36 partial status epilepticus patients, 11 (31%) showed thalamic lesions, and PLEDs were observed in all of the 11 patients. In addition, PLEDs were observed in 17 (68%) of the 25 patients not showing thalamic lesions.5
That study reported that there was no statistical association between PLEDs and thalamic lesions, and rather thalamic lesions were associated with brain lesions in posterior parts such as occipital lobe, parietal lobe, and temporal lobe and with the continuity of seizure. Also, it reported that among the thalamic nuclei the pulvinar appeared to be the structure playing the most important role in signal transduction. In DWI of these cases, cortical lesions were more extensive in patient 1 who had lesions in the pulvinar than in patient 2, and the seizure in EEG lasted longer in patient 1. These findings were similar to previous reports.
It has not been clarified whether PLEDs, which were described for the first time in 1964, are caused by epileptic seizure or are secondary events caused by lesions.7
PLEDs have been reported in patients with stroke, brain tumor, epilepsy, herpes encephalitis, metabolic encephalopathy, etc., and particularly in connection to epilepsy, they are known to be related to clinical seizure and it is believed that they occur due to disconnection between deep intracerebral structures such as basal nuclei and thalamus and cerebral cortex. In the patient of our case as well, along with ipsilateral extensive cortical and thalamic lesions, PLEDs of 0.5–1 Hz were observed in the hemisphere of the same side in EEG. As the patient’s consciousness decreased while PLEDs were observed, it was thought to suggest a state of non-convulsive seizure. Although previous studies failed to prove a statistical association between PLEDs and thalamic lesion,5
and there was a report in Korea that PLEDs were not observed in a non-convulsive status epilepticus patient who had thalamic lesions,8
it may be hard to exclude completely the association between the thalamus and PLEDs in status epilepticus in consideration that all of status epilepticus patients with thalamic lesions showed PLEDs in previous studies and in this case as well.5
Patient 1, who was a chronic alcoholic, can be classified into the category of subacute encephalopathy with seizure in alcoholics (SESA). SESA is a disease of a chronic alcoholic characterized by seizure along with local neurologic disorder, and PLEDs in EEG, and is known to cause status epilepticus.9
In patient 1, local neurologic disorder was not found clearly but SESA was suspected in the patient because of the history of chronic alcoholism, elevation of liver enzyme levels in serologic test, and PLEDs in EEG. Patient 2, without a history of alcoholism, had shown right parietal lobe epilepsy, and as it was aggravated with the stopping of medication, the patient had shown continuous partial seizure and intermittent generalized seizure. The patient’s seizure focus was believed to be the right parietal lobe showing high signal intensity in DWI, and crossed cerebellar diaschisis was observed, but lesions were not observed in the pulvinar and PLEDs were not observed in EEG.
This case report compared a patient having lesions in the cerebral cortex and pulvinar, crossed cerebellar diaschisis, and PLEDs with a status epilepticus patient who showed only lesions in the cerebral cortex and crossed cerebellar diaschisis with neither pulvinar lesions nor PLEDs observed. In a status epilepticus patient, crossed cerebellar diaschisis or signal enhancement in the thalamus may happen in brain MRI due to the overactivity or disorder of seizure-related cortex and pathway connected to them. Such brain imaging findings tend to appear more frequently in status epilepticus patients with uncontrollable or long-lasting seizure, and in particular thalamic lesions are believed to be related to the progression of seizure.